Home About us Contact
|
Home About us Contact | ||
|
|
||
Surfactant Therapy (surfactant + therapy)
Selected AbstractsOvercoming surfactant inhibition with polymersACTA PAEDIATRICA, Issue 12 2000PA Dargaville Inhibition of the function of pulmonary surfactant in the alveolar space is an important element of the pathophysiology of many lung diseases, including meconium aspiration syndrome, pneumonia and acute respiratory distress syndrome. The known mechanisms by which surfactant dysfunction occurs are (a) competitive inhibition of phospholipid entry into the surface monolayer (e.g. by plasma proteins), and (b) infiltration and destabilization of the surface film by extraneous lipids (e.g. meconium-derived free fatty acids). Recent data suggest that addition of non-ionic polymers such as dextrano and polyethylene glycol to surfactant mixtures may significantly improve resistance to inhibition. Polymers have been found to neutralize the effects of several different inhibitors, and can produce near-complete restoration of surfactant function. The anti-inhibitory properties of polymers, and their possible role as an adjunct to surfactant therapy, deserve further exploration. [source] Treatment of Premature Calves with Clinically Diagnosed Respiratory Distress SyndromeJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2008T. Karapinar Background: Respiratory distress syndrome (RDS) has been reported previously in premature calves. However, there have been no published data on the effect of surfactant replacement therapy in the treatment of premature calves with RDS. Hypothesis: Surfactant replacement therapy added to the standard treatment for premature calves clinically diagnosed with RDS would increase the viability of the calves. Animals: Twenty-seven premature calves with clinically diagnosed RDS. Methods: Twenty calves were instilled intratracheally with bovine lung surfactant extract and provided with standard treatment for RDS (surfactant group). Seven calves were given only standard care for RDS without surfactant therapy and placed in the control group. Standard treatment for newborn calves with RDS includes warming, administration of intranasal oxygen, fluid replacement, administration of antibiotics, and immunoglobulin solution. Arterial blood samples were collected from the calves at 3 observation points, the first just before treatment (hour 0) and at 2 hours (hour 2) and 24 hours (hour 24) after treatment was started to determine if ventilation was adequate, improving, or deteriorating. Blood gases, pH, bicarbonate, and lactate concentrations were measured. Results: In the surfactant group, mean partial pressure of oxygen significantly increased at hours 2 and 24. Mean partial pressure of carbon dioxide decreased and mean arterial blood pH increased at hour 24 in the surfactant group compared with the control group (P < .05). Of the 20 calves in the surfactant group, 12 survived and 8 died. All 7 calves in the control group died. Conclusions and Clinical Importance: The results of this study suggest that surfactant replacement therapy may reduce neonatal deaths in premature calves with clinically diagnosed RDS. [source] Changes in arterial oxygen tension when weaning neonates from inhaled nitric oxide,,PEDIATRIC PULMONOLOGY, Issue 1 2001Gregory M. Sokol MD Abstract We set out to evaluate changes in arterial oxygen tension (PaO2) when weaning neonates from inhaled nitric oxide (INO). We reviewed the records of 505 prospectively collected INO weaning attempts on 84 neonates with hypoxic respiratory failure. PaO2 values before and 30 min after weaning attempts were recorded. Relationships between change in PaO2 and decreases in INO concentrations were investigated using regression analysis and ANOVA. PaO2 decreased (,18.7,±,1.8 torr; P,<,0.001); when weaning INO. A stepwise decline in PaO2 was observed weaning INO from 40 ppm. The greatest decline occurred when INO was discontinued (,42.1,±,4.1 torr). Forward stepwise multiple regression using variables with significant relationships to the decline in PaO2 identified the specific dose reduction 7(P,<,0.001), the prewean PaO2 (P,<,0.001), and surfactant therapy (P,=,0.018) as the variables best describing the change in PaO2(P,=,0.004, r,=,0.51). In conclusion, a graded decline in PaO2 occurs when reducing INO. INO should be weaned to less than 1 ppm before discontinuing its use. Prior surfactant treatment appears to enhance the oxygenation reserve when weaning INO. Pediatr Pulmonol. 2001; 32:14,19. © 2001 Wiley-Liss,Inc. [source] Parental and perinatal factors affecting childhood anthropometry of very-low-birth-weight premature infants: a population-based surveyACTA PAEDIATRICA, Issue 6 2009Imad R Makhoul Abstract Background: The perinatal,neonatal course of very-low-birth-weight (VLBW) infants might affect their childhood growth. We evaluated the effect of parental anthropometry and perinatal and neonatal morbidity of VLBW neonates on their childhood growth. Methods: We obtained parental anthropometry, height and weight at age 6,10.5 years of 334 children born as VLBW infants. Parental, perinatal and neonatal data of these children were tested for association with childhood anthropometry. Results: (1) Maternal and paternal weight standard deviation score (SDS) and discharge weight (DW) SDS were associated with childhood weight SDS (R2= 0.111, p < 0.00001); (2) Maternal and paternal height SDS, corrected gestational age (GA) at discharge, maternal assisted reproduction and SGA status were associated with childhood height SDS (R2= 0.208, p < 0.00001); (3) paternal weight SDS, DW SDS and surfactant therapy were associated with childhood body mass index (BMI) SDS (R2= 0.096, p < 0.00001). 31.1% of VLBW infants had DW SDS < ,1.88, and are to be considered small for gestational age (,SGA'). One quarter of these infants did not catch up by age 6,10.5 years. Conclusion: Childhood anthropometry of VLBW infants depends on parental anthropometry, postnatal respiratory morbidity and growth parameters at birth and at discharge. Almost one-third of VLBW premature infants had growth restriction at discharge from neonatal intensive care unit (NICU), a quarter of whom did not catch up by age 6,10.5 years. [source] A randomized trial comparing beractant and poractant treatment in neonatal respiratory distress syndromeACTA PAEDIATRICA, Issue 6 2005Colleen Ann Malloy Abstract Aim: To compare the effects of beractant and poractant in neonatal respiratory distress syndrome (RDS). Methods: Infants with RDS were randomized to receive beractant or poractant. The primary outcome measure was fraction of inspired oxygen (FiO2) requirement in the first 48 h after surfactant therapy. Results: 58 infants completed the study. The mean gestational ages for the poractant and beractant groups were 29.6±3.6 and 29.3±2.9 wk, with average birthweights of 1394±699 and 1408±534 g, respectively. In the first 48 h, infants who received poractant had a lower FiO2 requirement compared to those who received beractant (p=0.018). The prevalence of patent ductus arteriosus (PDA) was lower in the group of infants that received poractant (17%) compared to the group that received beractant (45%) (p=0.02). Conclusions: Infants with RDS treated with poractant had a lower FiO2 requirement during the first 48 h compared to infants who received beractant. Infants who received poractant also had fewer PDAs than infants who received beractant. The difference in FiO2 was not associated with a difference in age of first extubation, total intubation time, or incidence of bronchopulmonary dysplasia between groups. [source] In-hospital mortality of newborn infants born before 33 weeks of gestation depends on the initial level of neonatal care: the EPIPAGE studyACTA PAEDIATRICA, Issue 3 2003JP Empana Aim: To determine the relation between the level of initial neonatal care and in-hospital mortality of infants born before 33 wk of gestation in the era of surfactant therapy. Methods: A 1 y prospective population-based survey was conducted in the north of France, as part of the EPIPAGE (Epidemiologie des Petits Ages Gestationnels) survey. Perinatal data were recorded for 585 very premature newborns transferred to a neonatal intensive care unit in 1997. The relation between the level of the neonatal unit that provided care for the first consecutive 48 h and in-hospital mortality was assessed by multivariate logistic regression, and adjusted for perinatal data and initial disease severity, estimated by the Clinical Risk Index for Babies (CRIB). Results: The average gestational age (mean ± SD) was 31.6 ± 0.62 wk in level I, 30.7 ± 0.21 in level II, 29.9 ± 0.13 in non-teaching level III, and 29.0 ± 0.15 in the level III teaching unit (p < 0.0001). The mean in-hospital mortality rate was 8.4% and did not differ by level of care (ptrend= 0.17). After adjustment for perinatal data and CRIB, however, with the teaching unit as the reference, the risk of death was significantly higher in level I,II units [adjusted odds ratio (ORa) = 7.9, 95% confidence interval (95% CI) 2.2,29.1], but not in the non-teaching level III units (ORa = 0.8, 95% CI 0.3,2.1). Conclusion: In-hospital mortality in non-teaching level III units was similar to that in a teaching unit, but significantly higher in level I-level II units. Neonatal care of newborns delivered before 33 wk of gestation should initially occur in level III units. [source] | ||||||||||